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Understanding the response and tolerance mechanisms of nitrogen (N) stress is essential for the taproot plant of sugar beet. Hence, in this study, low (0.5 and 3 mmol/L; N0.5 and N3), moderate (5 mmol/L; N5; control) and high (10 and 12 mmol/L; N10 and N12) N were imposed to sugar beet to comparatively investigate the growth and physiological changes, and expression pattern of the gene involving ammonia transporting at different seedling stages. The results showed that, different from N5 which could induce maximum biomass of beet seedlings, low N was more likely to inhibit the growth of beet seedlings than high N treatments. Morphological differences and adverse factors increased significantly with extension of stress time, but sugar beet seedlings displayed a variety of physical responses to different N concentrations to adapt to N abnormal. At 14 d, the chlorophyll content, leaf and root surface area, total dry weight and nitrogen content of seedlings treated with N0.5 decreased 15.83%, 53.65%, 73.94%, 78.08% and 24.88% respectively, compared with N12; however, the root shoot ratio increased significantly as well as superoxide dismutase (SOD), peroxidase (POD), glutamine synthetase (GS) activity and malondialdehyde (MDA) and proline content, especially in root. The expression of BvAMT1.2 was also regulated in an N concentration-dependent manner, and was mainly involved in the tolerance of beet leaves to N stress, which significantly positively correlated to GS activity on the basis of its high affinity to N. It can be deduced that the stored nutrients under low N could only maintain relatively stable root growth, and faced difficulty in being transported to the shoots. Sugar beet was relatively resilient to N0.5 stress according to the mean affiliation function analysis. These results provide a theoretical basis for the extensive cultivation of sugar beet in N-stressed soil.

Extraversion is the best and most consistent predictor of important leadership outcomes. However, there has been little exploration and examination of the mechanisms underlying the effects of extraverted leadership on performance. Drawing on distal-proximal motivational theory and situational strength theory, the present study proposes and examines a moderated mediation model that explains how leader extraversion affects team performance and how situational characteristics strengthen or constrain this relationship. Respondents were recruited through management team training courses run by the eight Chinese companies. We conducted two rounds of electronic questionnaire collection. The first round of data was collected during the training session. Four weeks later, we collected the data through the training courses' WeChat groups. Data collected from 226 Chinese team leaders was analyzed using SPSS 26 and Mplus 7. We find that leader extraversion predicts team performance through a motivational mechanism operationalized as leader work engagement. We further find that goal clarity and process clarity play an important role in strengthening the positive effect of leader extraversion on leader work engagement as well as the motivational mechanism, providing an empirical explanation of how leader extraversion affects team performance through a motivational mechanism operationalized as leader work engagement. We also explore how two potential situational characteristics, operationalized as goal clarity and process clarity of leaders, affect the relationship between leader extraversion and leader work engagement as well as the motivational mechanism. Addionally, the findings suggest important practical implications for the organizations seeking to identify effective team leaders.

Comprehending heavy mineral composition of the sandy land in Northeast China (NESL) is of great significance for interpreting generation, pathways, source and geochemistry of sediments in this area. To this end, the fine-grained (

The carcinogen urethane induces pulmonary tumors in mice initiated by an incredibly specific Q61L/R oncogenic mutation in the proto-oncogene Kras. Previous Whole-Exome Sequencing of urethane-induced tumors revealed a bias towards A➙T/G and G➙A substitutions. Subsequent ultra-sensitive Maximum-Depth Sequencing of Kras shortly after urethane exposure suggest a further refinement to CA➙CT/G substitutions. As C182AA➙C182T/GA substitutions in Kras result in Q61L/R mutations, the extreme bias of urethane towards these genomic driver mutations can be ascribed to the specificity of the carcinogen for CA➙CT/G substitutions. However, we previously found that changing rare codons to common in the Kras gene to increase protein expression shifted mutations in urethane-induced tumors away from Kras, or when detected in Kras, to G12D mutations that are usually rarely detected in such tumors. Moreover, the loss of p53 partially reversed this effect, generating tumors with either Q61L/R or G12D oncogenic Kras mutations, or no Kras mutations, presumably due to other genomic driver mutations. Determining the origin of these G12D and other unknown non-canonical genomic driver mutations would provide critical insight into the extreme bias of carcinogens for specific genomic driver mutations. We thus compared the types of Single Nucleotide Variations detected by previously performed Maximum-Depth Sequencing immediately after urethane exposure to the mutation signatures derived from Whole Exome Sequencing of urethane-induced tumors. This identified two types of non-canonical mutations. First, a V637E oncogenic mutation in the proto-oncogene Braf that conforms to the mutation signature of urethane, suggesting that the mutational bias of the carcinogen may account for this non-canonical mutation, similar to that for canonical Q61L/R mutations in Kras. Second, G12D and Q61H mutations in Kras that did not fit this mutation signature, and instead shared similarity with Single Nucleotide Variations detected by Maximum-Depth Sequencing from normal cells, suggesting that perhaps these mutations were pre-existing. We thus posit that when canonical Kras mutations are selected against that the carcinogen may instead promote the expansion of pre-existing genomic driver mutations, although admittedly we cannot rule out other mechanisms. Interrogating the mutation signatures of human lung cancers similarly identified KRAS genomic driver mutations that failed to match the mutation signature of the tumor. Thus, we also speculate that the selection for non-canonical genomic driver mutations during urethane carcinogenesis may reflect the process by which discordance between genomic driver mutations and mutational signatures arises in human cancers.

Wild relatives represent a source of variation for many traits of interest for eggplant (Solanum melongena) breeding, as well as for broadening its genetic base. However, interspecific hybridization with wild relatives has been barely used in eggplant breeding programs, and reproductive barriers have resulted in reduced seed numbers in interspecific combinations. The mechanism underlying this phenomenon remains unclear. We hybridized females of cultivated eggplant 177 (Solanum melongena) with males of wild relatives 53 and Y11 (Solanum aethiopicum). Self-crossed 177 was the control. The seed number per control fruit was significantly higher than that of the hybrids. Paraffin sections showed no significant difference between control and 177×53 and 177×Y11. Double fertilization began 4 days post-pollination. Sperm cells were fused with egg cells 6 days post-pollination. To understand the differences in molecular mechanisms underlying this process, transcriptomes of ovaries at 0, 4, and 6 days after self-crossing and hybridization were analyzed. We screened 22,311 differentially expressed genes (DEGs) between the control and hybrids 4 and 6 days post-pollination. A total of 497 DEGs were shared among all pollination combinations. These DEGs were enriched in plant hormone transduction, cell senescence, metabolism, and biosynthesis pathways. DEG clustering analysis indicated distinct expression patterns between the control and hybrids but not between the hybrids. The DEGs in hybrids involved secondary metabolic process, phenylpropanoid metabolic process, and carboxypeptidase activity, while those in the control involved xyloglucan metabolic process, auxin-activated signaling pathway, cell wall polysaccharide metabolic process, and xyloglucosyl transferase activity. Additionally, 1683 transcription factors, including members of the AP2-ERF, MYB, bHLH, and B3 families may play important roles in self-crossing and hybridization. Our results provide insights into the regulatory mechanisms underlying variations between ovaries of self-crossed and hybrid eggplants and a basis for future studies on crossbreeding Solanum and genetic mechanisms underlying double fertilization.

Fluorescent proteins and epitope tags are often used as protein fusion tags to study target proteins. One prevailing technique in the budding yeast Saccharomyces cerevisiae is to fuse these tags to a target gene at the precise chromosomal location via homologous recombination. However, several limitations hamper the application of this technique, such as the selectable markers not being reusable, tagging of only the C-terminal being possible, and a "scar" sequence being left in the genome. Here, we describe a strategy to solve these problems by tagging target genes based on a pop-in/pop-out and counter-selection system. Three fluorescent protein tag (mCherry, sfGFP, and mKikGR) and two epitope tag (HA and 3×FLAG) constructs were developed and utilized to tag HHT1, UBC13 or RAD5 at the chromosomal locus as proof-of-concept.

Duck enteritis virus (DEV) can infect ducks, geese, and many other poultry species and leads to acute, septic and highly fatal infectious disease. Autophagy is an evolutionarily ancient pathway that plays an important role in many viral infections. We previously reported that DEV infection induces autophagy for its own benefit, but how this occurs remains unclear. In this study, endoplasmic reticulum (ER) stress was triggered by DEV infection, as demonstrated by the increased expression of the ER stress marker glucose-regulated protein 78 (GRP78) and the dilated morphology of the ER. Pathways associated with the unfolded protein response (UPR), including the PKR-like ER protein kinase (PERK) and inositol-requiring enzyme 1 (IRE1) pathways, but not the activating transcription factor 6 (ATF6) pathway, were activated in DEV-infected duck embryo fibroblast (DEF) cells. In addition, the knockdown of both PERK and IRE1 by small interfering RNAs (siRNAs) reduced the level of LC3-II and viral yields, which suggested that the PERK-eukaryotic initiation factor 2α (eIF2α) and IRE1-x-box protein1 (XBP1) pathways may contribute to DEV-induced autophagy. Collectively, these data offer new insight into the mechanisms of DEV -induced autophagy through activation of the ER stress-related UPR pathway.